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Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children

Multisystem inflammatory syndrome in children (MIS-C) is a rare pediatric inflammatory disorder characterized by immune cell hyperactivation, cytokine storm, and the production of autoantibodies. The mechanisms underlying such immune dysregulation still need to be unraveled. In this issue of the JCI...

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Detalles Bibliográficos
Autores principales: Noval Rivas, Magali, Arditi, Moshe
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Society for Clinical Investigation 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9797332/
https://www.ncbi.nlm.nih.gov/pubmed/36594470
http://dx.doi.org/10.1172/JCI166016
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author Noval Rivas, Magali
Arditi, Moshe
author_facet Noval Rivas, Magali
Arditi, Moshe
author_sort Noval Rivas, Magali
collection PubMed
description Multisystem inflammatory syndrome in children (MIS-C) is a rare pediatric inflammatory disorder characterized by immune cell hyperactivation, cytokine storm, and the production of autoantibodies. The mechanisms underlying such immune dysregulation still need to be unraveled. In this issue of the JCI, Benamar et al. demonstrated the critical role of the Notch receptor 1/CD22 (Notch1/CD22) axis in Tregs, which, when activated, impairs Treg functions and promotes inflammation. They showed that the Notch1/CD22 axis contributed to dysregulated immune responses in MIS-C. These findings may have implications for MIS-C and many other inflammatory diseases.
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spelling pubmed-97973322023-01-10 Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children Noval Rivas, Magali Arditi, Moshe J Clin Invest Commentary Multisystem inflammatory syndrome in children (MIS-C) is a rare pediatric inflammatory disorder characterized by immune cell hyperactivation, cytokine storm, and the production of autoantibodies. The mechanisms underlying such immune dysregulation still need to be unraveled. In this issue of the JCI, Benamar et al. demonstrated the critical role of the Notch receptor 1/CD22 (Notch1/CD22) axis in Tregs, which, when activated, impairs Treg functions and promotes inflammation. They showed that the Notch1/CD22 axis contributed to dysregulated immune responses in MIS-C. These findings may have implications for MIS-C and many other inflammatory diseases. American Society for Clinical Investigation 2023-01-03 /pmc/articles/PMC9797332/ /pubmed/36594470 http://dx.doi.org/10.1172/JCI166016 Text en © 2023 Rivas et al. https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Commentary
Noval Rivas, Magali
Arditi, Moshe
Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children
title Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children
title_full Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children
title_fullStr Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children
title_full_unstemmed Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children
title_short Notch1 signaling impairs regulatory T cells during multisystem inflammatory syndrome in children
title_sort notch1 signaling impairs regulatory t cells during multisystem inflammatory syndrome in children
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9797332/
https://www.ncbi.nlm.nih.gov/pubmed/36594470
http://dx.doi.org/10.1172/JCI166016
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